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ABSTRACT: Spinal cord stimulation (SCS) is becoming a widely used treatment for a number of pain conditions and is frequently considered as a pain management option when conservative or less invasive techniques have proven to be ineffective. Potential indications for SCS include complex regional pain syndrome (CRPS), postherpetic neuralgia, traumatic nerve injury, failed back surgery syndrome, refractory angina pectoris, peripheral vascular disease, neuropathic pain, and visceral pain (Guttman et al. Pain Pract. 9:308-11, 2009). While research on SCS is in its infancy, it is clear that substantial variation exists in the degree of benefit obtained from SCS, and the procedure does not come without risks; thus focused patient selection is becoming very important. Psychological characteristics play an important role in shaping individual differences in the pain experience and may influence responses to SCS, as well as a variety of other pain treatments (Doleys Neurosurg Focus 21:E1, 2006). In addition to psychological assessment, quantitative sensory testing (QST) procedures offer another valuable resource in forecasting who may benefit most from SCS and may also shed light on mechanisms underlying the individual characteristics promoting the effectiveness of such procedures (Eisenberg et al. Pain Pract. 6:161-165, 2006). Here, we present a brief overview of recent studies examining these factors in their relationship with SCS outcomes.
Current Pain and Headache Reports 01/2013; 17(1):307. · 1.66 Impact Factor
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ABSTRACT: INTRODUCTION: Fibromyalgia (FM), characterized by wide-spread diffuse pain and sensory abnormalities, is associated with elevated indices of distress and pain-related catastrophizing compared to both pain-free samples and those with chronic pain conditions. Catastrophizing is a pervasive negative mental set, and is a strong predictor of negative pain-related outcomes such as clinical pain intensity, and physical disability. Situational catastrophizing, measured in the context of experimentally-induced pain, is strongly related to enhanced pain sensitivity, a core aspect of the pathophysiology of fibromyalgia. However, little is known regarding the temporal course of the association between catastrophizing and pain-related "outcomes". Most studies involve only static assessments of pain and catastrophizing at a single time point, which provides little insight into the direction of the observed associations. We sought to investigate the temporal relationships between catastrophizing and indices of both clinical pain (substudy 1) and experimentally-induced pain (substudy 2) in a larger randomized control longitudinal trial. METHODS: Fifty-seven patients with FM completed catastrophizing, depression, and pain questionnaires as well as laboratory cold pressor pain testing at baseline, post-intervention and three month follow-up during a lifestyle physical activity study. Cross-lagged panel analyses were used to address these temporal relationships. RESULTS: In substudy 1, analyses revealed that pre-to-post changes in dispositional catastrophizing ratings prospectively accounted for unique variance in subsequent post-to-follow-up changes in clinical pain ratings (p = 0.005), while pre-to-post changes in pain ratings did not account for unique variance in post-to-follow-up changes in catastrophizing ratings. An identical pattern was observed experimentally in substudy 2, with pre-to-post changes in situational catastrophizing ratings prospectively accounting for unique variance in subsequent post-to-follow-up changes in experimental pain ratings (p = 0.014), while pre-to-post changes in pain ratings did not account for unique variance in post-to-follow-up changes in catastrophizing ratings. Specifically, initial alterations in catastrophizing were associated with subsequent alterations in clinical and experimentally induced pain. Controlling for levels of depression did not affect the results. CONCLUSIONS: These findings provide empirical evidence that catastrophizing processes might precede and contribute to subsequent alterations in the pain experience for FM patients.
Arthritis research & therapy 10/2012; 14(5):R231. · 4.27 Impact Factor
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ABSTRACT: OBJECTIVE: Radiographic measures of knee osteoarthritis (K-OA) pathology have modest associations with clinical pain. We sought to evaluate possible differences in quantitative sensory testing (QST), and psychosocial distress profiles between K-OA patients with discordant versus congruent clinical pain reports relative to radiographic severity measures. PATIENTS AND METHODS: 113 participants (67% women, Mean age = 61.05 ± 8.93) with K-OA participated in the study. Radiographic joint pathology was graded via the Kellgren-Lawrence scale. Central sensitization was indexed through quantitative sensory testing, including heat and pressure pain threshold, tonic suprathreshold pain (cold pressor test), and repeated phasic suprathreshold mechanical and thermal pain. Subgroups were constructed by dichotomizing clinical knee pain scores (median split) and knee grade scores (1-2 vs. 3-4), resulting in four groups: Low Pain/Low Knee Grade (n=24), High Pain/Low Knee Grade (n=30), Low Pain/High Knee Grade (n=27), and High Pain/High Knee Grade (n=32). RESULTS: Multivariate analyses revealed significantly heightened pain sensitivity in the High Pain/Low Knee Grade group, while the Low Pain/High Knee Grade group was less pain sensitive. Group differences remained significant after adjusting for differences on psychosocial measures, as well as age, sex, and race. CONCLUSION: The results suggest that central sensitization in K-OA is especially apparent among patients with high clinical pain reports in the absence of moderate to severe radiographic evidence of K-OA pathology.
Arthritis & Rheumatism 09/2012; · 7.87 Impact Factor
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ABSTRACT: Robust interindividual variation in pain sensitivity has been observed, and recent evidence suggests that some of the variability may be genetically mediated. Our previous data revealed significantly higher pressure pain thresholds among individuals possessing the minor G allele of the A118G SNP of the mu-opioid receptor gene (OPRM1) compared with those with 2 consensus alleles. Moreover, ethnic differences in pain sensitivity have been widely reported. Yet, little is known about the potential interactive associations of ethnicity and genotype with pain perception. This study aimed to identify ethnic differences in OPRM1 allelic associations with experimental pain responses. A total of 247 healthy young adults from three ethnic groups (81 African Americans; 79 non-white Hispanics; and 87 non-Hispanic whites) underwent multiple experimental pain modalities (thermal, pressure, ischemic, cold pressor). Few African Americans (7.4%) expressed the rare allele of OPRM1 compared to non-Hispanic whites and Hispanics (28.7% vs. 27.8%, respectively). Across the entire sample, OPRM1 genotype did not significantly affect pain sensitivity. However, analysis in each ethnic group separately revealed significant genotype effects for most pain modalities among non-Hispanic-whites (P<.05) but not Hispanics or African Americans. The G allele was associated with decreased pain sensitivity among whites only; a trend in the opposite direction emerged in Hispanics. The reasons for this dichotomy are unclear; they may involve ethnic differences in haplotypic structure, or A118G may be a tag-SNP linked to other functional polymorphisms. These findings demonstrate an ethnicity-dependent association of OPRM1 genotype with pain sensitivity. Additional research is warranted to uncover the mechanisms influencing these relationships.
Pain 06/2012; 153(8):1610-9. · 5.78 Impact Factor
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Jeffrey S Mogil,
Robert E Sorge,
Michael L LaCroix-Fralish,
Shad B Smith,
Anny Fortin,
Susana G Sotocinal,
Jennifer Ritchie,
Jean-Sebastien Austin,
Ara Schorscher-Petcu,
Kara Melmed, [......], Claudia M Campbell,
Robert R Edwards,
James N Campbell,
Jacqueline N Crawley,
William R Lariviere,
Margaret R Wallace,
Wendy F Sternberg,
Carey D Balaban,
Inna Belfer,
Roger B Fillingim
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ABSTRACT: Quantitative trait locus mapping of chemical/inflammatory pain in the mouse identified the Avpr1a gene, which encodes the vasopressin-1A receptor (V1AR), as being responsible for strain-dependent pain sensitivity to formalin and capsaicin. A genetic association study in humans revealed the influence of a single nucleotide polymorphism (rs10877969) in AVPR1A on capsaicin pain levels, but only in male subjects reporting stress at the time of testing. The analgesic efficacy of the vasopressin analog desmopressin revealed a similar interaction between the drug and acute stress, as desmopressin inhibition of capsaicin pain was only observed in nonstressed subjects. Additional experiments in mice confirmed the male-specific interaction of V1AR and stress, leading to the conclusion that vasopressin activates endogenous analgesia mechanisms unless they have already been activated by stress. These findings represent, to the best of our knowledge, the first explicit demonstration of analgesic efficacy depending on the emotional state of the recipient, and illustrate the heuristic power of a bench-to-bedside-to-bench translational strategy.
Nature Neuroscience 12/2011; 14(12):1569-73. · 15.53 Impact Factor
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ABSTRACT: Sleep quality and ethnicity are related to a host of general health outcomes including the experience of pain, yet it remains unclear whether poor sleep quality and ethnicity might interactively affect pain catastrophizing and laboratory-evoked acute pain reports. The current study examined the cross-sectional associations of subjective sleep quality, ethnicity, and their interaction with pain catastrophizing and pain reports.
Healthy (N = 149), ethnically diverse (58% Caucasian American, 23% Asian American, 19% African American) young adults were subjected to a cold pressor task (CPT). Prior to CPT, participants completed the Pittsburgh Sleep Quality Index and a standard version of the Pain Catastrophizing Scale (PCS). Following CPT, participants completed a situation-specific version of the PCS.
Adjusted analyses revealed a significant sleep quality by ethnicity interaction for standard catastrophizing reports. Particularly, African Americans with poor overall sleep quality reported the greatest level of catastrophizing on the standard PCS relative to their Caucasian American and Asian American counterparts. Furthermore, African Americans with poorer sleep efficiency reported greater catastrophizing on the situation-specific PCS compared with Caucasian American and Asian Americans. Catastrophizing was significantly correlated with pain reports.
These results suggest that African Americans with poorer sleep quality may be at greater risk for catastrophizing, a known contributor to more intense pain and increased pain-related emotional distress. Whether interventions that improve the sleep quality of ethnic minorities affect pain catastrophizing is in need of investigation.
Pain Medicine 06/2011; 12(6):913-22. · 2.35 Impact Factor
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ABSTRACT: Opioids have become the unequivocal therapy of choice in treating many varieties of chronic pain. With the increased prescription of opioids, some unintended consequences have occurred. After prolonged opioid exposure, opioid-induced hyperalgesia (OIH), the paradoxical effect that opioid therapy may in fact enhance or aggravate preexisting pain, may occur. Over the past several decades, an increasing number of laboratory and clinical reports have suggested lowered pain thresholds and heightened atypical pain unrelated to the original perceived pain sensations as hallmarks of OIH. However, not all evidence supports the clinical importance of OIH, and some question whether the phenomenon exists at all. Here, we present a nonexhaustive, brief review of the recent literature. OIH will be reviewed in terms of preclinical and clinical evidence for and against its existence; recommendations for clinical evaluation and intervention also will be discussed.
Current Pain and Headache Reports 01/2011; 15(2):129-36. · 1.66 Impact Factor
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ABSTRACT: OBJECTIVES: The aim of this prospective investigation was to evaluate ethnic group differences in pain-related outcomes following multidisciplinary chronic pain treatment. A prospective pre- and post-treatment assessment design was employed to investigate the effects of ethnicity on changes in pain-related variables following completion of a multidisciplinary pain treatment program. METHODS: One hundred fifty five chronic pain patients participating in a multidisciplinary pain treatment program completed measures of pain and mood both prior to and following the four-week treatment. Primary outcome variables included pain severity, pain-related interference, and depressive symptoms. RESULTS: Baseline differences between African-Americans and Whites were observed for depressive symptoms, but not for pain severity or pain-related interference. Following multidisciplinary pain treatment, both White and African-American patients displayed post-treatment reductions in depressive symptoms and pain-related interference. However, White patients also reported reduced pain severity while African-Americans did not. CONCLUSIONS: The treatment approach used in the present study appeared to be less effective in reducing self-reported pain severity in African-American versus White patients, though both groups benefited in terms of reduced depressive symptoms and pain-related interference. Moreover, the observation that improvements in functioning occurred without reductions in pain severity in African-American patients suggests that differences may exist in treatment processes as a function of ethnic group, and will consequently be an important area for future research.
Journal of Musculoskeletal Pain 01/2011; 19(1):24-30. · 0.35 Impact Factor
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ABSTRACT: Although sleep deprivation is known to heighten pain sensitivity, the mechanisms by which sleep modifies nociception are largely unknown. Few studies of sleep-pain interactions have utilized quantitative sensory testing models that implicate specific underlying physiologic mechanisms. One possibility, which is beginning to receive attention, is that differences in sleep may alter the analgesic effects of distraction. We utilized the heat-capsaicin nociceptive model to examine whether self-reported habitual sleep duration is associated with distraction analgesia, the degree of secondary hyperalgesia and skin flare, markers implicating both central and peripheral processes that heighten pain. Twenty-eight healthy participants completed three experimental sessions in a randomized within subjects design. In the pain only condition, pain was induced for approximately 70-min via application of heat and capsaicin to the dorsum of the non-dominant hand. Verbal pain ratings were obtained at regular intervals. In the distraction condition, identical procedures were followed, but during heat-capsaicin pain, subjects played a series of video games. The third session involved assessing performance on the video games (no capsaicin). Participants indicated their normal self-reported habitual sleep duration over the past month. Individuals who slept less than 6.5 h/night in the month prior to the study experienced significantly less behavioral analgesia, increased skin flare and augmented secondary hyperalgesia. These findings suggest that reduced sleep time is associated with diminished analgesic benefits from distraction and/or individuals obtaining less sleep have a reduced ability to disengage from pain-related sensations. The secondary hyperalgesia finding may implicate central involvement, whereas enhanced skin flare response suggests that sleep duration may also impact peripheral inflammatory mechanisms.
European journal of pain (London, England) 12/2010; 15(6):561-7. · 3.37 Impact Factor
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ABSTRACT: Considerable evidence has linked catastrophizing to pain responses, and recent experimental pain research has suggested that situational catastrophizing, measured during or immediately after laboratory pain procedures, is strongly related to pain ratings of standardized noxious stimuli. However, given that most experimental pain protocols involve "static" assessments of pain ratings and catastrophizing at a single time point, the direction by which these factors may affect each other remains unclear. Does catastrophizing influences one's subsequent pain responses or do individual differences in the perceived severity of pain lead to differential rates of catastrophizing? Little is known regarding the course of these variables. Using a cross-lagged panel analysis, we evaluated whether changes in situation-specific catastrophizing preceded changes in laboratory-induced pain responses, or vice versa, during tonic capsaicin pain stimulation. Topical application of a 10% capsaicin cream was applied to the dorsal aspect of the nondominant hand of 38 healthy participants. Situation-specific catastrophizing and pain ratings were obtained at Early (0 to 15 minutes), Mid (15 to 30 minutes), and Final (30 to 35 minutes) periods during capsaicin pain. Analyses revealed that Early-to-Mid changes in catastrophizing ratings prospectively accounted for unique variance in subsequent Mid-to-Final changes in pain ratings, whereas Early-to-Mid changes in pain ratings did not account for unique variance in Mid-to-Final changes in catastrophizing ratings. That is, participants who showed the largest initial increases in catastrophizing reported the greatest subsequent increases in pain. Controlling for the reported change in stress did not affect this pattern of results. These findings provide empirical evidence that a situation-specific catastrophizing process might precede and contribute to subsequent increases in pain experience. Limitations of the present study and possible future research directions are discussed. PERSPECTIVE: The present study adds to a growing literature on prospective associations between catastrophizing and pain. These results provide initial evidence, in healthy individuals, that changes in catastrophizing may precede changes in pain response.
The journal of pain: official journal of the American Pain Society 09/2010; 11(9):876-84. · 3.78 Impact Factor
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ABSTRACT: Catastrophizing is widely recognized as an important risk factor for adverse pain-related outcomes. However, questions remain surrounding the details of its assessment. In particular, recent laboratory studies suggest that evaluation of "situational" catastrophizing (ie, catastrophizing measured during or directly after the administration of noxious stimulation) may provide information distinct from that obtained by standard, or "dispositional" measures, which assess individuals' recall of catastrophizing in daily life. However, comparatively little research has systematically investigated the interrelationships and properties of these 2 different forms of pain-related catastrophizing. The current study evaluated both situational and dispositional catastrophizing measures within multiple samples: healthy individuals (N = 84), patients with painful temporomandibular joint disorders (TMD; N = 48), and patients with painful arthritis (N = 43). All participants first completed the Pain Catastrophizing Scale (PCS), and then underwent psychophysical pain testing, which included heat, cold, and pressure pain. Participants then completed a situational catastrophizing measure with reference to the laboratory pain he/she had just undergone. Situational catastrophizing scores were not significantly correlated with dispositional PCS scores in the healthy participants and arthritis patients, though they were associated in TMD patients. Situational catastrophizing was more strongly associated with experimental pain responses than dispositional PCS scores for the healthy subjects and arthritis patients. In general, higher levels of situational catastrophizing were associated with lower pain thresholds and higher pain ratings across all 3 samples. The findings highlight the importance of multidimensional assessment of pain-related catastrophizing, and suggests a role for measuring catastrophizing related to specific, definable events. PERSPECTIVE: This study adds to a growing literature examining catastrophizing. Our findings highlight the potential importance of the multidimensional assessment of pain-related catastrophizing, and suggest a role for measuring catastrophizing related to specific, definable events.
The journal of pain: official journal of the American Pain Society 05/2010; 11(5):443-453.e2. · 3.78 Impact Factor
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ABSTRACT: Behavioral analgesic techniques such as distraction reduce pain in both clinical and experimental settings. Individuals differ in the magnitude of distraction-induced analgesia, and additional study is needed to identify the factors that influence the pain relieving effects of distraction. Catastrophizing, a set of negative emotional and cognitive processes, is widely recognized to be associated with increased reports of pain. We sought to evaluate the relationship between catastrophizing and distraction analgesia. Healthy participants completed three sessions in a randomized order. In one session (Pain Alone), pain was induced by topical application of a 10% capsaicin cream and simultaneous administration of a tonic heat stimulus. In another session (Pain+Distraction), identical capsaicin+heat application procedures were followed, but subjects played video games that required a high level of attention. During both sessions, verbal ratings of pain were obtained and participants rated their degree of catastrophizing. During the other session (Distraction Alone) subjects played the video games in the absence of any pain stimulus. Pain was rated significantly lower during the distraction session compared to the "Pain Alone" session. In addition, high catastrophizers rated pain significantly higher regardless of whether the subjects were distracted. Catastrophizing did not influence the overall degree of distraction analgesia; however, early in the session high catastrophizers had little distraction analgesia, though later in the session low and high catastrophizers rated pain similarly. These results suggest that both distraction and catastrophizing have substantial effects on experimental pain in normal subjects and these variables interact as a function of time.
Pain 02/2010; 149(2):202-7. · 5.78 Impact Factor
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Pain Medicine 10/2009; · 2.35 Impact Factor
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ABSTRACT: The side effects of opioids have been widely investigated, but it is unknown whether the subjective effects of mu agonists and mixed action opioids produce similar symptom profiles. This study examined the structure and predictive validity of somatic and cognitive/affective side-effect profiles of morphine and pentazocine using the Somatic Side Effects Questionnaire and the Cognitive and Affective Side Effects Questionnaire.
The subjects were 122 female and 90 male healthy volunteers that received an intravenous bolus administration of either 0.08 mg/kg of morphine or 0.5 mg/kg pentazocine. Pre- and post-drug experimental pain testing was also performed. Exploratory and confirmatory factor analysis resulted in similar factor structures for both drugs.
The most frequently reported side effects across both drugs involved feeling relaxed, sedation, and feeling in control. At equianalgesic doses, pentazocine had greater aversive side effects than morphine, whereas morphine was more associated with feelings of control and euphoria. For both drugs, females reported greater frequency of negative side effects than males. Using cluster analysis, we identified similar symptom profiles for each drug. These drug-related side-effect profiles were linked with analgesic responses. Specifically, groups that had a more positive side-effect profile experienced the greatest analgesic effect based on changes in ischemic pain sensitivity.
These findings have implications for decisions regarding opioid management of acute, chronic, and malignant pain conditions.
Pain Medicine 09/2009; 11(2):195-206. · 2.35 Impact Factor
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ABSTRACT: Pain catastrophizing is conceptualized as a negative cognitive-affective response to anticipated or actual pain and has been associated with a number of important pain-related outcomes. In the present review, we first focus our efforts on the conceptualization of pain catastrophizing, highlighting its conceptual history and potential problem areas. We then focus our discussion on a number of theoretical mechanisms of action: appraisal theory, attention bias/information processing, communal coping, CNS pain processing mechanisms, psychophysiological pathways and neural pathways. We then offer evidence to suggest that pain catastrophizing represents an important process factor in pain treatment. We conclude by offering what we believe represents an integrated heuristic model for use by researchers over the next 5 years; a model we believe will advance the field most expediently.
Expert Review of Neurotherapeutics 06/2009; 9(5):745-58.
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ABSTRACT: The well-accepted biopsychosocial model proposes that the experience of pain and responses to it result from a complex interaction of biological, psychological, and social factors. However, the separation of these constructs is substantially artificial, and we presume that psychological processes have biological effects, that biological processes affect an individual's psychosocial environment, and so on. Considerable research has demonstrated that pain-coping strategies influence perceived pain intensity and physical functioning, and individual differences in styles of pain coping even shape the persistence of long-term pain complaints in some populations. A good deal of this coping research has focused on catastrophizing, which is a generally maladaptive cognitive and emotional mental set that involves feelings of helplessness when in pain, rumination about pain symptoms, and magnification of pain-related complaints. Collectively, catastrophizing has been consistently associated with heightened experiences of pain across a variety of samples. Although catastrophic thinking regarding pain-related symptoms is often classified under the "psychologic" category within the broader biopsychosocial model, we propose that catastrophizing exerts biologic effects that may account for some of its negative consequences. In general, the cognitive and affective processes captured within the construct of catastrophizing may exert effects on the neuromuscular, cardiovascular, immune, and neuroendocrine systems, and on the activity in the pain neuromatrix within the brain. The interface between pain-related neurobiology and processes such as pain-related catastrophizing represents an important avenue for future pain research.
Translational Research 04/2009; 153(3):97-101. · 2.99 Impact Factor
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ABSTRACT: Objective. This review highlights research on sex-based differences in pain perception and treatment. We sought to illuminate the complex factors contributing to differences in pain and analgesic responses between males and females, ranging from psychosocial to biological processes.Design. We reviewed published studies of pain induction by chemical, electric, heat, surgical, or psychological means, and opioid and nonopioid analgesia comparing responses in men and women.Results. A substantial body of research indicates that women experience greater clinical pain, suffer greater pain-related distress, and show heightened sensitivity to experimentally induced pain compared with men. Research on sex-based differences in the pain experience and treatment is beginning to uncover patterns that may enable tailoring of pain treatment to individual characteristics. The factors underpinning sex differences in the experience of pain are multifactorial and complex; for example, psychosocial factors such as pain-related catastrophizing may explain sex-based differences in reporting certain types of pain, as women tend to use catastrophizing to a greater degree. Gonadal hormone levels in cycling women also have a substantial impact on pain perception and analgesic response. Women perceive more pain during the luteal phase, and estrogen antagonists provide long-term pain relief in certain situations.Conclusions. Collectively, greater understanding of the factors that commonly and differentially affect the disparity in pain perception, as well as analgesic response, are beginning to illuminate research targets and promising areas of therapeutic intervention for improved pain management.
Pain Medicine 02/2009; 10(2):289 - 299. · 2.35 Impact Factor
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ABSTRACT: This review highlights research on sex-based differences in pain perception and treatment. We sought to illuminate the complex factors contributing to differences in pain and analgesic responses between males and females, ranging from psychosocial to biological processes.
We reviewed published studies of pain induction by chemical, electric, heat, surgical, or psychological means, and opioid and nonopioid analgesia comparing responses in men and women.
A substantial body of research indicates that women experience greater clinical pain, suffer greater pain-related distress, and show heightened sensitivity to experimentally induced pain compared with men. Research on sex-based differences in the pain experience and treatment is beginning to uncover patterns that may enable tailoring of pain treatment to individual characteristics. The factors underpinning sex differences in the experience of pain are multifactorial and complex; for example, psychosocial factors such as pain-related catastrophizing may explain sex-based differences in reporting certain types of pain, as women tend to use catastrophizing to a greater degree. Gonadal hormone levels in cycling women also have a substantial impact on pain perception and analgesic response. Women perceive more pain during the luteal phase, and estrogen antagonists provide long-term pain relief in certain situations.
Collectively, greater understanding of the factors that commonly and differentially affect the disparity in pain perception, as well as analgesic response, are beginning to illuminate research targets and promising areas of therapeutic intervention for improved pain management.
Pain Medicine 02/2009; 10(2):289-99. · 2.35 Impact Factor
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ABSTRACT: Though it is clear that genomic variability plays an integral role in accounting for pain sensitivity, controversy exists over which genes are involved. While recent data suggest a "protective" (i.e., less pain) haplotype in the GTP cyclohydrolase (GCH1) gene, other research has failed to confirm this association. Possibly, the effects of single nucleotide polymorphisms (SNPs) vary depending on the pain task. The current investigation analyzed the association of five previously identified GCH1 SNPs with ratings of pain induced by topical high concentration (10%) capsaicin applied to the skin of 39 healthy human volunteers. Each of the GCH1 polymorphisms was associated with lower pain ratings. When combined, three of the five accounted for a surprisingly high 35% of the inter-individual variance in pain ratings. We conclude that SNPs of the GCH1 gene may profoundly affect the ratings of pain induced by capsaicin.
Pain 01/2009; 141(1-2):114-8. · 5.78 Impact Factor
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ABSTRACT: Substantial evidence indicates that the experience of both clinical and experimental pain differs among ethnic groups. Specifically, African Americans generally report higher levels of clinical pain and greater sensitivity to experimentally induced pain; however, little research has examined the origins of these differences. Differences in central pain-inhibitory mechanisms may contribute to this disparity. Diffuse noxious inhibitory controls (DNIC), or counterirritation, is a phenomenon thought to reflect descending inhibition of pain signals. The current study assessed DNIC in 57 healthy young adults from 2 different ethnic groups: African Americans and non-Hispanic whites. Repeated assessments of the nociceptive flexion reflex (NFR) as well as ratings of electrical pain were obtained before, during, and after an ischemic arm pain procedure (as well as a sham procedure). The DNIC condition (ie, ischemic arm pain) produced substantial reductions in pain ratings as well as electrophysiologic measures of the NFR for all participants when compared with the sham condition (P < .001). The DNIC condition produced significantly greater reductions in verbal pain ratings among non-Hispanic whites when compared with African Americans (P = .02), whereas ethnic groups showed comparable reductions in NFR. The findings of this study suggest differences in endogenous pain inhibition between African Americans and non-Hispanic whites and that additional research to determine the mechanisms underlying these effects is warranted. PERSPECTIVE: This study adds to the growing literature examining ethnic differences in experimental pain perception. Our data suggest that these variations may be influenced by differences in descending inhibition.
The journal of pain: official journal of the American Pain Society 05/2008; 9(8):759-66. · 3.78 Impact Factor
